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Biomedical subjects

K Stollhoff

Publications and source records attributed to K Stollhoff.

6 recordsLinked to original sources

Development and perinatal risk factors of very low-birth-weight infants. Small versus appropriate for gestational age.

371 long-term surviving very low-birth-weight (VLBW) infants born between July 1983 and June 1986 with a birthweight under 1501 g were followed-up. This sample amounted to 91% of such infants of six neonatal intensive care units in Hamburg (Germany). A neurological examination and a developmental evaluation using the Griffith Developmental Scale were carried out at the age of 18 to 20 months, corrected for gestational age. Ninety-six of the 371 infants were small for gestational age (SGA), 275 appropriate for gestational age (AGA). Striking differences between these two groups were found concerning perinatal risk factors and neurological outcome. Maternal risk factors associated with intrauterine growth retardation such as maternal toxemia and signs of fetal stress were found in a high percentage of the mothers of SGA-children, factors associated with premature labor and chorioamnionitis in mothers of AGA-children. Cerebral palsy was detected in only 7% of the SGA-children but 17.5% of the AGA-children. The difference in the development of cerebral palsy was attributed mainly to different postconceptual ages of the SGA- and AGA-children. In general, minor neurological abnormalities were detected in as many as 30% of SGA- and only 15.3% of AGA-children. None of the SGA-children over 33 weeks of gestational age developed cerebral palsy, but 25% minor neurological abnormalities. As to cerebral palsy the prognosis of SGA-infants with a very low birthweight is not different from AGA-infants with a similar gestational age. Regarding the development of minor neurological abnormalities, however, intrauterine growth retardation seems to be a risk factor independent from gestational age.

Attention Deficit Disorder with Hyperactivity↗

Development of very low birth weight infants: a regional study of 371 survivors.

We re-examined 371 infants with birth weights less than 1501 g at a corrected age of 18-20 months. This sample amounted to 91% of such infants admitted to one of the six neonatal intensive care units in Hamburg between July 1983 and 1986. The neurological examination and a developmental evaluation using the Griffith Developmental Scale revealed higher rates of abnormalities than in most other studies. Fifty-five children (14.8%) suffered from cerebral palsy, classified in 45 as spastic diplegia, in 5 as spastic tetraplegia, in 1 as spastic hemiplegia and in 4 as dystonia. Of the children, 41 (11%) showed minor neurological deviations (hyperactivity, clumsiness, intention tremor). The development of 30 children (8%) without neurological abnormalities was moderately retarded (DQ 80-89, corrected for gestational age [GA]). Nineteen children (5%) were severely retarded (DQ less than 80, corrected for GA) and four children (1.5%) were blind due to retrolental fibroplasia. An isolated delay of speech development was found in 5 children. Seventy children (18.9%) had a major and 87 children (23.5%) a minor handicap.

Cerebral Palsy↗

Vitamin B12 and brain development.

This is a report of a 1 1/2-year-old male with megaloblastic anaemia and a progressive neurological disorder clinically resembling leucodystrophy. The child was exclusively breast fed and his mother had been a strict vegetarian for more than 4 years before the child was born. After Vitamin B12 therapy the anaemia disappeared and the neurological condition dramatically improved.

Anemia, Macrocytic↗

Shock and terminal pancreatitis.

63% of 523 lethal cases of shock showed a DIC-syndrome. First of all the lung was affected with 69% of the cases with DIC-syndrome, followed by the pancreas with 52%. In search of disseminated intravascular coagulation, the pancreas is a very favourable organ since other acute superimposed findings normally don't exist. 18% of the cases with DIC-syndrome showed in addition to the DIC-syndrome a terminal pancreatitis resp. a tryptic necrosis. The pathogenesis of the tryptic necrosis can be explained by a decrease of blood supply in shock, which makes autodigestion possible. The tryptic necrosis differs from the hypoxic necrosis phenomenologically. The hypoxia as pathogenetic principle (Franz Büchner) causes the tryptic necrosis in an indirect way: it provides the conditions for autodigestion. This study aims to encourage to examine the pancreas of lethal cases of shock more regularly since this examination is an enrichment as well for the anatomic diagnosis of shock as for the comprehension of the pancreas.

Disseminated Intravascular Coagulation↗

Giant axonal neuropathy and leukodystrophy.

An 11-year-old Persian boy, born to consanguineous parents, manifested a progressive gait abnormality beginning at 5 years of age. A severe cerebellar disorder developed with associated dysfunction of the peripheral nervous system, but no sign of mental impairment. The sensory and motor nerve conduction velocities were greatly reduced, especially in the lower extremities. Cerebrospinal fluid protein was normal. Computed tomography and magnetic resonance imaging revealed leukoencephalopathy, especially in the cerebellum, but also in periventricular areas. The diagnosis of giant axonal neuropathy was established by biopsy of the sural nerve. The few previous histologic examinations have documented hyperplasia of the microfibrils which accumulate in the axons as well as in neurilemma, endothelial, and perineural cells. This is the first report of involvement of supraspinal portions of the central nervous system documented by postmortem examination after in vivo imaging methods corroborated the morphologic concomitants of the clinical symptoms.

Axons↗